| 引用本文: |
敖懿姿, 胡淑颖, 张婷玉, 孙鑫, 李小科.基于糖脂代谢重编程视角探讨糖肝共病“浊邪内伏”病机及辨治概要[J].湖南中医药大学学报,2025,45(8):1500-1505[点击复制] |
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| 基于糖脂代谢重编程视角探讨糖肝共病“浊邪内伏”病机及辨治概要 |
| 敖懿姿,胡淑颖,张婷玉,孙鑫,李小科 |
| (北京中医药大学东直门医院, 北京 100700;北京中医药大学肝病研究院, 北京 100700) |
| 摘要: |
| 2型糖尿病（T2DM）合并代谢相关脂肪性肝病（MAFLD）共病率逐年攀升，二者在糖脂代谢紊乱方面存在病理协同基础。根据《内经》所载“浊邪”凝聚伏匿的生理特性，结合糖肝共病的临床表现与病理特征，认为“浊邪内伏”为本病的病机核心，其内在病理基础在于糖脂代谢重编程，即糖脂稳态失调驱动代谢物异常堆积与毒化，表现为：秽浊初伏期胰岛素抵抗，诱导糖脂异生与脂肪酸摄取增加；浊邪壅滞期持续的代谢重编程，加速脂肪异位沉积、炎症因子释放及微循环障碍，驱动肝脏微环境由“瘀”转“浊”；浊毒损络期糖脂毒性、氧化应激加剧及晚期糖基化终产物形成，最终导致肝细胞损伤、纤维化及多系统并发症，即“络损脏衰”。遂提出本病三期辨治思路：秽浊初伏期以脾失散精、秽浊积生为初始，治宜健脾运、刮浊邪；浊瘀壅滞期以浊瘀互结、枢机不利为进展，治宜利枢机、通络滞；浊毒损络期以浊毒互滋、络损脏衰为终末，治宜化浊毒、疗脏损。本文旨在通过融合代谢重编程机制与“浊邪内伏”病机演化，为中医药防治糖肝共病提供新的理论依据与临床治疗思路。 |
| 关键词: 代谢相关脂肪性肝病 2型糖尿病 浊邪内伏 糖脂代谢重编程 分期辨治 |
| DOI：10.3969/j.issn.1674-070X.2025.08.015 |
| 投稿时间：2025-05-09 |
| 基金项目:国家自然科学基金面上项目(82174341);国家中医药管理局第七批全国老中医药专家学术经验继承工作(中国中医药人教函[2022]76号);世界中医药科技专项项目(WFCMS2024026) |
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| Pathogenesis of "internal retention of turbid pathogens" in T2DM-MAFLD comorbidity and its differentiation and treatment from the perspective of glycolipid metabolism reprogramming |
| AO Yizi, HU Shuying, ZHANG Tingyu, SUN Xin, LI Xiaoke |
| (Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China;Institute of Liver Diseases, Beijing University of Chinese Medicine, Beijing 100700, China) |
| Abstract: |
| The comorbidity rate of type 2 diabetes（T2DM） combined with metabolic associated fatty liver disease（MAFLD） has been steadily increasing year by year, with both conditions sharing a pathological synergy in glycolipid metabolic disorders.According to the physiological characteristics of "turbid pathogen" coagulation and concealment described in Huang Di Nei Jing（Huangdi’s Classic of Medicine）, combined with the clinical manifestations and pathological features of the co-morbidity of diabetes and liver diseases, it is believed that "internal retention of turbid pathogen" constitutes the core pathogenesis of this condition, with its intrinsic pathological basis lying in glycolipid metabolism reprogramming. This refers to the dysregulation of glycolipid homeostasis driving abnormal accumulation and toxicity of metabolites, manifesting as follows: during the initial stage of turbid pathogen retention, insulin resistance induces increased uptake of gluconeogenesis, lipogenesis, and fatty acid; in the stage of turbid pathogen stagnation, persistent metabolic reprogramming accelerates ectopic fat deposition, the release of inflammatory factors, and microcirculatory disturbances, driving the transition of hepatic microenvironment from "stasis" to "turbidity"; in the stage of turbid toxin damaging collaterals, intensified glycolipid toxicity and oxidative stress, and the formation of advanced glycation end（AGE）products ultimately lead to hepatocyte injury, fibrosis, and multisystem complications, namely "collateral damage and organ failure".Consequently, a three-stage differentiation and treatment approach for this condition is proposed: in the initial stage of turbid pathogen retention, characterized by spleen dysfunction in distributing essence and the accumulation of turbid pathogens, treatment should focus on invigorating the spleen to transport and transform nutrients and eliminating turbid pathogens; in the progressive stage of turbid pathogen and blood stasis stagnation, marked by the intertwining of turbid pathogens and blood stasis and impaired pivot mechanism, treatment should aim to regulate pivot mechanism and unblock collateral stagnation; in the terminal stage of turbid toxin damaging collaterals, characterized by the mutual nourishment of turbid pathogens and toxins and collateral damage leading to organ failure, treatment should focus on resolving turbid toxins and repairing organ damage. This article aims to provide a new theoretical basis and clinical treatment approach for Chinese medicine in preventing and treating the comorbidity of T2DM and MAFLD by integrating the mechanisms of metabolic reprogramming with the evolution of the pathogenesis of "internal retention of turbid pathogen". |
| Key words: metabolic associated fatty liver disease type 2 diabetes internal retention of turbid pathogen glycolipid metabolism reprogramming staged differentiation and treatment |
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